Reperfusion Injury After Hemorrhage: A Collective Review

G D. Rushing, MD; L D. Britt, MD, MPH


Annals of Surgery. 2008;247(6):929-937. 

In This Article

Mitochondrial Oxidative Metabolism and Reperfusion Injury

Associated with high-energy phosphate production and oxygen consumption, mitochondria have been defined as the workhorse of the cell. Mitochondria consume greater than 90% of cellular oxygen.[59] In patients undergoing resuscitation, it has been noted that optimal delivery of oxygen does not result in increased utilization of that oxygen. Inability of the mitochondria to use oxygen, due to electron chain transport uncoupling, is a focus of ongoing investigation. This phenomenon of uncoupling has been termed cytopathic hypoxia.[60] Reperfusion injury diminishes the ability of mitochondria, utilizing the electron transport chain, to formulate adenosine triphosphate via oxidative phosphorylation. Ninety percent of oxygen consumption, along the electron transport chain, occurs at cytochrome a,a3 (also known as cytochrome c oxidase). Cytochrome c oxidase contributes to reperfusion injury through production of reactive oxygen species in the mitochondria.[25,61] Changes in the cellular redox state may modulate the cell's vulnerability to the inflammatory response in shock states. Nuclear factor kappa-B (NF-κB) is known to be a redox sensitive transcription factor with regards to the production of TNF-α. Mitochondrial respiration is important in activation of NF-κB and subsequent proinflammatory mediator production.[62,63]


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